Insulin's action on mammalian cells involve regulation of a number of vital metabolic functions and processes, e.g., glucose transport and utilization, lipogenesis and storage of fatty acids as acylglycerols, increased protein synthesis and antagonism of fatty acid mobilization. This variety of metabolic effects, termed "the pleiotypic effects" are subjected to a renewed evaluation since the first demonstration by us that insulin's effects on glucose oxidation or its antagonism of adenylate cyclase activity are regulated by a mechanism which is distinct from the activation of hexose transport. This is in concert with the previous reports that many important biological effects of insulin, e.g., the antilipolytic effect, are independent of glucose translocation. Although the hormone reacts exclusively with its specific receptors in the cellular plasma membrane, it may generate a single or multiple messenger molecules - to regulate the separate metabolic pathways within the cells. Previous attempts to identify any messenger system for this hormone were not successful. We have recognized an oxidase activity in the plasma membrane of the target cells, the adipocytes, which responds to insulin and leads to a drastic change in the cytoplasmic redox state. Our present aim is to identify, isolate and characterize the reaction cycle within the plasma membrane and in the cytoplasm which are triggered, subsequent to the hormone-receptor interaction, and to correlate these functions to the known loci of insulin-responsive reactions within these cells. Adipocytes are the most convenient model system for these studies, for their acute sensitivity to insulin, their relatively simple metabolic pattern and other hormones and their easy availability. We believe that identification and characterization of the reactive plasma membrane components and of their product(s) may finally elucidate the mechanism of action of this hormone and the molecular changes leading to insulin-resistance. This should help explore the conditions to reverse these diseases.